Bicuculline, a GABA receptor blocker, has been found to restore binocular input to neurons of the visual cortex of cats with monocular deprivation amblyopia. This appears incompatible with the "disuse atrophy" theory of amblyopia and has important practical applications. We suggest that loss of functioal input from the amblyopic eye is due to GABA mediated synaptic inhibition. We will test this hypothesis in cats by a combined neurophysiological, pharmacological, and biochemical approach. Our major objectives will be: 1) to determine if bicuculline acts to restore binocularity via blockade of GABA receptors; 2) to search for an effective but less toxic drug; 3) to search for evidence of synaptic inhibition of input from the amblyopic eye; 4) to find the $ locus or loci of action of bicuculline; 5) to find whether bicuculline restores functional vision to the deprived eye; 6) to explore the role of inhibition in visual abnormalities produced by asymmetries of the visual environment not involving deprivation; 7) to study the relationship between visual experience and the development of inhibition; 8) to determine whether the critical period can be modified by biochemical or environmental factors; 9) to seek biochemical correlates of the critical period; 10) to seek biochemical correlates of the postulated abnormal inhibition in amblyopia; 11) to correlate receptor distribution and properties with the abnormal physiology of amblyopia.